EP 345.038 describes the use of non-β-oxidizable fatty acid analogues of the formula;Alkyl-X—CH2COORwherein the alkyl is a saturated or unsaturated hydrocarbon chain of 8 to 22 carbon atoms, X represents a O, S, SO or SO2, and R is hydrogen or a C1-C4 alkyl group, for the treatment of hyperlipaemic conditions and for the reducing the concentration of cholesterol and triglycerides in the blood of mammals.
PCT/NO95/00195 describes alkyl-S—CH2COOR and alkyl-Se—CH2COOR for the inhibition of the oxidative modification of LDL. Further, this application describes the use of the selenium-compound for the treatment of hyperlipaemic condition and for reducing the concentration of cholesterol and trigylcerides.
The PCT applications PCT/NO99/00135, PCT/NO99/00136 and PCT/NO99/00149 describes fatty acid analogous of the formula (I)CH3—[CH2]m—[xi—CH2]n—COOR                wherein n is an integer from 1 to 12, and        wherein m is an integer from 0 to 23, and        wherein i is an odd number which indicates the position relative to COOR, and        wherein Xi independent of each other are selected from the group comprising O, S, SO, SO2, Se and CH2, and        wherein R represents hydrogen or C1-C4 alkyl,        with the proviso that at least one of the Xi is not CH2,or a salt, prodrug or complex thereof.        
This formula comprises one or several X groups (preferably selenium and sulphur) in positions 3, 5, 7, 9, etc.
Further, these PCT applications describe several medicinal and nutritional applications.
PCT/NO99/00135 describes the use of the fatty acid analogues the treatment and/or prevention of obesity, hypertension, fatty liver and the multi metabolic syndrome termed <<metabolic syndrome >> or Syndrome X. Further, this application describes a method for the treatment or prevention of an obese or overweight condition, and a method for producing weigh loss or a reduction of the fat mass in a human or non-human animal. The application also describes a nutritional composition effective to reduce, or to prevent an increase in, the total body weight or the total body fat mass in a human or non-human animal, and also a method for the modification of the fat distribution and content of animals in order to improve the quality of the meat, or product such as milk and eggs.
PCT/NO99/00136 describes use of fatty acid analogues for the treatment and/or prevention of diabetes (both type I and II), and a method for the treatment or prevention of hyperglycaemia, hyperinsulinemia and reduced sensitivity to insulin. A nutritional composition effective to reduce, or to prevent an increase in the concentration of glucose in the blood of a human or non-human animal is also disclosed, as is a method for reducing the concentration of glucose in the blood of a human or non-human animal.
PCT/NO99/00149 describes the use of the fatty acid analogues for the treatment and/or prevention of primary and/or secondary stenosis, and/or a disease caused by procedural vascular trauma and/or pathological proliferation of smooth muscle cells, and/or an increased level of plasma homocystein.
Due to the X-atom (most preferable sulphur or selenium) that is substituted in the carbon chain of the above given fatty acid analogues, these compounds will not be β-oxidized in the mitochondria beyond this position. Thus, the degradation of these molecules must start from the methyl end of the fatty acid, and this is a rather slow metabolic process. The catabolism of these fatty acid analogues includes ω-oxidation and chain shortening of the dicarboxylic acid by peroxisomes. Enzymes in the endoplasmic reticulum will ω-hydroxylate and further oxidise the hydroxylated fatty acid to a dicarboxylic acid. This acid may then be chain shortened by β-oxidation in the peroxisomes. Studies in rats have shown that 50% of the analogue TTA was excreted in the urine as short sulfoxy dicarboxylic acids within 24 hours of administration. In similar experiments it has been found that a desaturated product of TTA is formed in vivo. This is due to the microsomal enzyme Δ9-desaturase which inserts a double bond in the 9-position of saturated fatty acids.
It is anticipated that this desaturated product has similar effects, and/or mediates the biological effects of the saturated fatty acid analogues. It is also likely that the biological effects of fatty acid analogues may be potentiated by slowing down their catabolism. This can be done by inserting double and/or triple bonds near the methyl end of the fatty acids, and/or by incorporating alkyl groups or halogens in this part of the molecule. Such molecules, i.e. the compounds in accordance with the present invention, will not be substrates for the relevant microsomal enzymes.